Without any effective treatment currently available in the hospital to reduce or compensate for neuronal cell loss in Huntington disease, novel treatment approaches, Icotinib including gene transfer systems, are now being examined so as to produce potential biotherapeutics to inclined neuronal populations. While molecular mechanisms by which the extended poly glutamine region in huntingtin causes selective loss in striatal neurons in HD patients continue to be to be fully elucidated, interest has focused on improving neurodegeneration via involvement in common cell survival/ cell death mechanisms. Prior studies by the others and ourselves have shown variable development of medium spiny neuron survival in animal models of HD subsequent delivery of neurotrophic factors. Post mortem analysis of HD brains showing an increase Plastid in pro apoptotic proteins, and the induction of apoptosis by mutant huntingtin expression in vitro and in vivo, give support to a growing belief that programmed cell death mechanisms give rise to the progressive neurodegeneration observed in HD. Apoptotic death of medium spiny striatal neurons has also been previously shown to be caused by quinolinic acid, which has been popular to replicate degeneration to the selective HD of striatal projection neurons. More over the vulnerability to excitotoxic insult in the HD brain is formulated through mutant huntingtin induced potentiation of the NR2B D methyl n aspartate receptor subunit which these GABAergic projection neurons generally express. This development of NMDA receptor activity causes a rise in intracellular calcium levels making these angiogenesis in vitro nerves highly prone to innate, mitochondrial licensed apoptotic cell death. It’s, thus, likely that the management of apoptotic inhibitors or enhancement of endogenous anti apoptotic factors may be therapeutically very theraputic for HD patients by reducing caspase mediated cleavage of huntingtin, thus reducing the generation of toxic N terminal pieces, or via general enlargement of the nerves power to endure cellular tensions including NMDA receptor mediated signalling. Consequently, we hypothesised the anti apoptotic facets X associated inhibitor of apoptosis and Bcl xL may possibly provide neuroprotection against QA caused excitotoxicity and reduce the loss of medium spiny striatal neurons. The inhibition of caspases is normally performed by proteins known as Inhibitors of Apoptosis of which XIAP is the strongest, capable of inhibiting both initiator caspase 9, and the executioner caspases 3 and 7. Over expression of XIAP was shown by Xu and colleagues to boost survival of hippocampal CA1 neurons against ischemic induced apoptosis, therefore attenuating loss of spatialmemory.